Evidence map›Paper›PMID 36369365›Full record

ReviewApoptosis : an international journal on programmed cell death2023

Molecular mechanisms of cell death in bronchopulmonary dysplasia.

Xianhui Deng, Zhidan Bao, Xianpeng Yang, Yingzi Mei, Qin Zhou, Ailing Chen, Renqiang Yu, Yongjun Zhang

Abstract readReview
PubMed Publisher
In one paragraph

Review in Apoptosis : an international journal on programmed cell death, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed, 1 pooled it
6.4field-weighted citation impact, top 2% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

35 citing papers in PubMed, 1 synthesis or guideline pooled it, 47 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors at 4 institutions in 1 country.

Xianhui Deng *Department of Neonatology, Wuxi Maternity and Child Health Care Hospital, Wuxi School of Medicine, Jiangnan University, Wuxi, China.
Zhidan Bao *Department of Neonatology, Jiangyin People's Hospital of Nantong University, Wuxi, China.
Xianpeng YangDepartment of Neonatology, Wuxi Maternity and Child Health Care Hospital, Wuxi School of Medicine, Jiangnan University, Wuxi, China.
Yingzi MeiDepartment of Neonatology, Wuxi Maternity and Child Health Care Hospital, Wuxi School of Medicine, Jiangnan University, Wuxi, China.
Qin ZhouDepartment of Neonatology, Wuxi Maternity and Child Health Care Hospital, Wuxi School of Medicine, Jiangnan University, Wuxi, China.
Ailing ChenTranslational Medicine Laboratory, Research Institute for Reproductive Health and Genetic Diseases, The Affiliated Wuxi Maternity and Child Health Care Hospital of Nanjing Medical University, Wuxi, China. okchenailing@163.com.
Renqiang YuDepartment of Neonatology, Wuxi Maternity and Child Health Care Hospital, Wuxi School of Medicine, Jiangnan University, Wuxi, China. yurenqiang553@163.com.
Yongjun ZhangDepartment of Neonatology, Xinhua Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China. zhangyongjun@sjtu.edu.cn.
Jiangnan University · CNJiangyin People's Hospital · CNNanjing Maternity and Child Health Care Hospital · CNShanghai Jiao Tong University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Bronchopulmonary dysplasia (BPD) in neonates is the most common pulmonary disease that causes neonatal mortality, has complex pathogenesis, and lacks effective treatment. It is associated with chronic obstructive pulmonary disease, pulmonary hypertension, and right ventricular hypertrophy. The occurrence and development of BPD involve various factors, of which premature birth is the most crucial reason for BPD. Under the premise of abnormal lung structure and functional product, newborns are susceptible to damage to oxides, free radicals, hypoxia, infections and so on. The most influential is oxidative stress, which induces cell death in different ways when the oxidative stress balance in the body is disrupted. Increasing evidence has shown that programmed cell death (PCD), including apoptosis, necrosis, autophagy, and ferroptosis, plays a significant role in the molecular and biological mechanisms of BPD and the further development of the disease. Understanding the mode of PCD and its signaling pathways can provide new therapeutic approaches and targets for the clinical treatment of BPD. This review elucidates the mechanism of BPD, focusing on the multiple types of PCD in BPD and their molecular mechanisms, which are mainly based on experimental results obtained in rodents.

Indexed as

Bronchopulmonary DysplasiaHypertension, PulmonaryApoptosisFemaleHumansInfant, NewbornLungOxidative StressPregnancyAlkaliptosisApoptosisAutophagyBronchopulmonary dysplasiaCell deathNecroptosis(necroptotic)Pyroptosis

Identifiers

PMID36369365
OpenAlexW4308791123

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.